Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An opportunity to develop a new generation of methods for pain relief has arisen from recent advances in the neurobiology of pain. A variety of sensitive and reliable pain assessment methods are now available to facilitate clinical trials. Assessment tools that are suitable for young children are being developed, making analgesic research feasible in this group of patients.New analgesic methods may either block the action of neurochemical mediators of pain or promote endogenous pain-relieving systems. Treatments aimed at preventing peripheral nerve sensitization by inflammatory products avoid the side effects of centrally acting narcotic analgesics. Endogenous opioid systems are involved in the body's analgesic response to acute pain and stress. Pituitary beta-endorphin release is a likely component of this response and may be manipulated by pharmacological interventions. Noradrenergic and serotonergic pain-inhibiting systems may mediate the specific analgesia produced by amitriptyline in neuropathic pain states.
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PMID:Mechanisms of pain and analgesia. 1959 95

Pituitary adenylate cyclase-activating peptide-38 (PACAP38) and vasoactive intestinal peptide (VIP) belong to the same secretin-glucagon superfamily and are present in nerve fibers in dura and skin. Using a model of acute cutaneous pain we explored differences in pain perception and vasomotor responses between PACAP38 and VIP in 16 healthy volunteers in a double-blind, placebo-controlled, crossover study. All participants received intradermal injections of 200 pmol PACAP38, 200 pmol VIP and placebo into the volar forearm. Measurements included pain intensity on a visual analog scale (VAS), blood flow by laser Doppler flowmetry, visual flare and wheal. Pain intensities after PACAP38 and VIP were mild and limited to a short time of about 100 s after injection. The area under the VAS-time curve was larger following PACAP38 (P = 0.004) and VIP (P = 0.01) compared to placebo. We found no statistical difference in pain perception between PACAP38 and VIP. Skin blood flow increase, flare and wheal were larger after both PACAP38 (P = 0.011) and VIP (P = 0.001) compared to placebo. VIP induced a considerably larger increase in skin blood flow, flare and wheal than PACAP38 (P = 0.002). In conclusion, we found that peripheral nociceptive cutaneous responses elicited by PACAP38 and VIP are similar in healthy volunteers. This suggests that acute pain and vasomotor responses following intradermal injections of PACAP38 and VIP are primarily mediated by VPAC receptors.
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PMID:Cutaneous nociception and neurogenic inflammation evoked by PACAP38 and VIP. 2045 93